Mixed-location cerebral hemorrhage/microbleeds

Pasi, Marco; Charidimou, Andreas; Boulouis, Grégoire; Auriel, Eitan; Ayres, Alison; Schwab, Kristin; Goldstein, Joshua N.; Rosand, Jonathan; Viswanathan, Anand; Pantoni, Leonardo; Greenberg, Steven M.; Gurol, M. Edip

doi:10.1212/wnl.0000000000004797

Cited by 149 publications

(130 citation statements)

References 30 publications

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“…But with persistent long-term hypertension and the decline of renal function, the cortical and leptomeningeal arteries will eventually be damaged. This is in line with a recent observation by Pasi et al ( 37 ) that CMB with mixed deep and lobar locations were associated with vascular risk factors similar to hypertensive ICH and severe hypertension could be responsible for ICH or CMB in the lobar location that are generally thought to be associated with CAA. This should be even more true in patients with severe hypertension, poor-controlled diabetes, or end-stage CKD.…”

Section: Discussionsupporting

confidence: 92%

Association of Chronic Kidney Disease With Small Vessel Disease in Patients With Hypertensive Intracerebral Hemorrhage

et al. 2018

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BackgroundChronic kidney disease (CKD) has been closely associated with hypertension and stroke. Although studies have reported the relationship between CKD and cerebral small vessel disease (SVD), the link between CKD, hypertension, and SVD is uncertain. The aim of this study was to investigate the association between CKD and SVD in patients with strictly hypertensive intracerebral hemorrhage (ICH).Methods142 patients with acute hypertensive ICH were enrolled in this study. Magnetic resonance imaging was performed to assess imaging markers for SVD. Patients were categorized into three CKD groups based on the degree of kidney dysfunction [glomerular filtration rate (GFR) in milliliters per minute per 1.73 m2]: normal kidney function (GFR ≥ 90), mild kidney disease (60 ≤ GFR < 90), and moderate to severe kidney disease (GFR < 60).ResultsThe prevalence rate of mild and moderate to severe CKD was 50 and 14.8%, respectively. The stage of CKD was associated with history of chronic hypertension (p = 0.046) as well as the prevalence rate of overall and deep cerebral microbleed (CMB) (p = 0.001 and p = 0.002, respectively). The stage of CKD was a significant risk factor for deep white matter hyperintensity (WMH) (OR 1.848; 95% CI 1.022–3.343, p = 0.042), overall CMB (OR 2.628; 95% CI 1.462–4.724, p = 0.001), lobar CMB (OR 2.106; 95% CI 1.119–3.963, p = 0.021), and deep CMB (OR 2.237; 95% CI 1.263–3.960, p = 0.006), even after adjustment for confounders.ConclusionIn patients with hypertensive ICH, the prevalence of CKD is high even at the early stage of renal function impairment and is associated with the prevalence of CMB and deep WMH. These results reinforce the notion of a link between hypertensive vasculopathy, renal function impairment, and cerebral SVD.

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Section: Discussionsupporting

confidence: 92%

Association of Chronic Kidney Disease With Small Vessel Disease in Patients With Hypertensive Intracerebral Hemorrhage

et al. 2018

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“…HTN-SVD has been associated with various additional radiological findings, including deep cerebral microbleeds (CMBs) ( Figure 1B ), white matter disease (leukoaraiosis) ( Figure 1C ), and MRI-visible enlarged perivascular spaces (EPVS) ( Figure 1F ) in the basal ganglia [ 15 , 16 ]. Recently, mixed-ICH, which refers to combined deep and lobar hemorrhage, is suggested to be associated with vascular risk factors similar to hypertensive ICH, but demonstrates more severe parenchymal damage and higher ICH recurrence risk ( Figure 1D ) [ 17 , 18 ].…”

Section: Cerebral Small Vessel Diseases: Major Etiology Of Lacunar Inmentioning

confidence: 99%

“…Patients with multiple strictly lobar CMB (without associative ICH) had risk factors and neuroimaging profiles similar to CAA, and possess a 5% annual risk of developing first-time symptomatic ICH during follow-up [ 54 ]. In contrast, the ICH risk is reported as 2% per year in survivors of hypertensive ICH [ 17 , 55 ]. In patients with mixed-ICH ( Figure 1E ), which may represent the consequence of more severe underlying HTN-SVD, the ICH recurrence rate increases to 5.1% per year according to a recent study [ 17 ].…”

Section: Cerebral Small Vessel Diseases: Major Etiology Of Lacunar Inmentioning

confidence: 99%

“…In contrast, the ICH risk is reported as 2% per year in survivors of hypertensive ICH [ 17 , 55 ]. In patients with mixed-ICH ( Figure 1E ), which may represent the consequence of more severe underlying HTN-SVD, the ICH recurrence rate increases to 5.1% per year according to a recent study [ 17 ]. Thus, identifying the underlying microangiopathy is crucial, especially in situations where patients have an indication for antithrombotic use, to balance hemorrhagic versus ischemic risks.…”

Section: Cerebral Small Vessel Diseases: Major Etiology Of Lacunar Inmentioning

confidence: 99%

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Updates on Prevention of Hemorrhagic and Lacunar Strokes

et al. 2018

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Intracerebral hemorrhage (ICH) and lacunar infarction (LI) are the major acute clinical manifestations of cerebral small vessel diseases (cSVDs). Hypertensive small vessel disease, cerebral amyloid angiopathy, and hereditary causes, such as Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL), constitute the three common cSVD categories. Diagnosing the underlying vascular pathology in these patients is important because the risk and types of recurrent strokes show significant differences. Recent advances in our understanding of the cSVD-related radiological markers have improved our ability to stratify ICH risk in individual patients, which helps guide antithrombotic decisions. There are general good-practice measures for stroke prevention in patients with cSVD, such as optimal blood pressure and glycemic control, while individualized measures tailored for particular patients are often needed. Antithrombotic combinations and anticoagulants should be avoided in cSVD treatment, as they increase the risk of potentially fatal ICH without necessarily lowering LI risk in these patients. Even when indicated for a concurrent pathology, such as nonvalvular atrial fibrillation, nonpharmacological approaches should be considered in the presence of cSVD. More data are emerging regarding the presentation, clinical course, and diagnostic markers of hereditary cSVD, allowing accurate diagnosis, and therefore, guiding management of symptomatic patients. When suspicion for asymptomatic hereditary cSVD exists, the pros and cons of prescribing genetic testing should be discussed in detail in the absence of any curative treatment. Recent data regarding diagnosis, risk stratification, and specific preventive approaches for both sporadic and hereditary cSVDs are discussed in this review article.

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“…ICH is thought to arise from rupture of arteries with diminished microvascular integrity due to either hypertensive arteriopathy, affecting deep perforating arterioles, or cerebral amyloid angiopathy, affecting cortical and leptomeningeal vessels [3,15]. Reflecting the distribution of the underlying type of microangiopathy, the former causes ICH's in deep and infratentorial locations, while the latter is associated with ICH's occurring in lobar regions [16,17]. It has been hypothesized that the diffuse cerebral vasculopathies associated with CSVD might allow for more extensive acute-phase bleeding and therefore influence the cascade of events once an ICH has occurred, theoretically leading to larger hemorrhage volumes, risk of hemorrhage expansion, and more extensive IVH [18].…”

Section: Introductionmentioning

confidence: 99%

Associations of Radiographic Cerebral Small Vessel Disease with Acute Intracerebral Hemorrhage Volume, Hematoma Expansion, and Intraventricular Hemorrhage

et al. 2019

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Background and Objective: The aim of this study was to evaluate the impact of radiographic cerebral small vessel disease (CSVD) on the severity of acute intracerebral hemorrhage (ICH) as measured by: ICH volume, hematoma expansion, and extension of intraventricular hemorrhage (IVH). Methods: CSVD was determined on baseline computed tomography (CT) scans of patients from the Ethnic and Racial Variations of Intracerebral Hemorrhage study through the extent of leukoaraiosis and cerebral atrophy using visual rating scales. The associations of leukoaraiosis and atrophy with ICH volume, hematoma expansion, IVH presence, and severity of IVH were tested using multivariable regression models. Secondary analyses were stratified by hemorrhage location. Bonferroni correction was applied to correct for multiple testing. Results: A total of 2579 patients (mean age 61.7 years, 59% male) met inclusion criteria. Median ICH volume was 10.5 (Interquartile range [IQR] 4.0-25.3) mL. IVH was detected in 971 patients (38%). Neither leukoaraiosis nor atrophy was associated with hematoma expansion. Increasing grades of leukoaraiosis were associated with increased risk of IVH in a dose-dependent manner, while cerebral atrophy was inversely associated with IVH (both P for trend < 0.001). Increasing grades of global atrophy were dose-dependently associated with lower ICH volumes (ß (95% Confidence Interval [CI]) − 0.30[− 0.46, − 0.14], − 0.33[− 0.49, − 0.17], − 0.40[− 0.60, − 0.20], and − 0.54[− 0.76, − 0.32], for grades 1, 2, 3 and 4 compared to 0; all P < 0.001). The associations of leukoaraiosis with ICH volume were consistent with those of atrophy, albeit not meeting statistical significance. Conclusions: Leukoaraiosis and cerebral atrophy appear to have opposing associations with ICH severity. Cerebral atrophy correlates with smaller ICH volume and decreased risk and severity of IVH, while leukoaraiosis is associated with increased risk of IVH. Whether these observations reflect overlapping or divergent underlying mechanisms requires further study.

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Mixed-location cerebral hemorrhage/microbleeds

Abstract: Mixed ICH, commonly seen on MRI obtained during etiologic workup, appears to be driven mostly by vascular risk factors similar to HTN-ICH but demonstrates more severe parenchymal damage and higher ICH recurrence risk.

Cited by 149 publications

References 30 publications

Association of Chronic Kidney Disease With Small Vessel Disease in Patients With Hypertensive Intracerebral Hemorrhage

Association of Chronic Kidney Disease With Small Vessel Disease in Patients With Hypertensive Intracerebral Hemorrhage

Updates on Prevention of Hemorrhagic and Lacunar Strokes

Associations of Radiographic Cerebral Small Vessel Disease with Acute Intracerebral Hemorrhage Volume, Hematoma Expansion, and Intraventricular Hemorrhage

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